What’s New in Cirrhotic Cardiomyopathy?—Review Article

Abstract

Cirrhotic cardiomyopathy (CCM) is a relatively new medical term. The constant development of novel diagnostic and clinical tools continuously delivers new data and findings about this broad disorder. The purpose of this review is to summarize current facts about CCM, identify gaps of knowledge, and indicate the direction in which to prepare an updated definition of CCM. We performed a review of the literature using scientific data sources with an emphasis on the latest findings. CCM is a clinical manifestation of disorders in the circulatory system in the course of portal hypertension. It is characterized by impaired left ventricular systolic and diastolic dysfunction, and electrophysiological abnormalities, especially QT interval prolongation. However, signs and symptoms reported by patients are non-specific and include reduced exercise tolerance, fatigue, peripheral oedema, and ascites. The disease usually remains asymptomatic with almost normal heart function, unless patients are exposed to stress or exertion. Unfortunately, due to the subclinical course, CCM is rarely recognized. Orthotopic liver transplantation (OLTx) seems to improve circulatory function although there is no consensus about its positive effect, with reported cases of heart failure onset after transplantation. Researchers indicate a careful pre-, peri-, and post-transplant cardiac assessment as a crucial point in detecting CCM and improving patients’ prognosis. There is also an urgent need to update the CCM definition and establish a diagnostic algorithm for early diagnosis of CCM as well as a specific treatment of this condition.

Cardiac Dysfunction and Its Relation to Degree of Esophageal Varices in Cirrhotic Patients

“…had CCM, and in group III, 7 (35%) patients had CCM, with no significant difference between the three groups. The previously mentioned data is demonstrated in Table (4).…”

“…A comparison of the criteria for the diagnosis of CCM is shown in Table (1). [4] Regarding the pathophysiology of CCM, it has been suggested that a hyperdynamic circulation initially compensates for the significant splanchnic arterial vasodilatation seen in liver cirrhosis; subsequently, liver disease progression and portal hypertension leads to additional splanchnic vasodilatation and a reduced effective arterial blood volume, which triggers the sympathetic nervous system and the renin-angiotensin-aldosterone system. Overexposure to sympathetic effector molecules results in downregulation, internalization, and cardiac damage, which impairs the function of β-adrenergic receptors [5].…”

Cardiomyopathy in cirrhosis: From pathophysiology to clinical care

“…with oxygen therapy, sodium restriction, and diuretics. 105 Besides reducing the risk of bleeding from oesophageal varices, 106 β-blockers alleviate systemic inflammation by reducing portal pressure, mesenteric venous congestion and intestinal permeability, thereby reducing the entry of inflammatory cytokines into the circulation. The alleviation of systemic inflammation may benefit the heart.…”

Cardiac risk stratification of the liver transplant candidate: A comprehensive review

“…PRS complicates 8%-30% of LT and manifests as dramatic reductions in the heart rate, cardiac output and systemic vascular resistance, leading to systemic hypotension, and in some cases dysrhythmias or even cardiac arrest[ 16 ]. Although the pathogenesis of PRS remains unclear, different mechanisms have been implicated with most important being the rapid release of vasoactive substances and pro-inflammatory cytokines [tumor necrosis factor (TNF)-1α, interleukin (IL)-6] from both the donor graft and the recipient’s immune system[ 16 , 17 ].…”